Investigation of the mechanism of EGFR-TKI resistance and establishment of new treatment strategy

2015 Fiscal Year Final Research Report

• Project/Area Number: 25860643
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Respiratory organ internal medicine
• Research Institution: Kobe University
• Principal Investigator: Tamura Daisuke 神戸大学, 医学部附属病院, 助教 (80646597)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 薬剤耐性クローン / EGFR-TKI / がん幹細胞 / 老化細胞

Outline of Final Research Achievements

Pathway-targeted cancer drug therapies can effectively produce dramatic responses. However, these therapies are not curative and the relatively rapid emergence of drug-tolerant persisters (DTPs) substantially limits the overall therapeutic benefit. This study aimed to clarify the varying composition of DTPs in EGFR mutated non-small lung cancer cells and to develop an effective treatment. Using FACS analysis, DTPs could be separated by CD133 expression pattern. CD133 high population expressed higher stem cell related markers and had other stem cell like properties. On the other hand, CD133 low population exhibited higher expression of cellular senescence associated proteins. Wthaferin A eliminated CD133 high cells effectively. In addition, inhibitors of a highly glucose-consuming condition suppressed CD133 low population emergence.

Free Research Field

呼吸器内科